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New case of BSE in Canada

18 Nov, 2008 06:41 AM
The Canadian Food Inspection Agency has announced that a seven-year-old dairy cow in British Columbia has been confirmed to have bovine spongiform encephalopathy (BSE or mad cow disease).

CFIA is conducting an investigation.

The birth farm has been identified and the animal's herdmates are being traced.

Possible sources of infection are also being explored.

According to the CFIA, the age and location of the cow are consistent with other cases detected in Canada.

The cow was found by the BSE surveillance program.

Because Canada was classified as a Controlled Risk country for BSE, CFIA says this case should not affect exports of Canadian cattle or beef.

R-CALF USA is again calling for USDA to withdraw the over the 30 months of age rule for importing Canadian cattle.

"USDA can no longer operate with its head in the sand when it comes to Canada’s BSE problems," said R-CALF USA CEO Bill Bullard.

"This makes the fourth case of Canadian BSE in 2008, and the sixth Canadian case in animals born in 2000-2001."

USDA officially declared the Canadian feed ban began on 1 March 1999.

This is the ninth case of BSE in a cow that would be eligible for importation into the U.S.

"It is beyond ridiculous for our government to continue to ignore the obvious risks with Canadian cattle and to put US beef consumers at risk," Mr Bullard said.

"As well as risking damage to the reputation of independent US cattle producers and the reputation of the safe, wholesome product they have worked so hard to promote."

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However,according to my opinion mad cow disease (BSE) is not an infectious disease. See my recent presentation at 29th World Veterinary Congress in Vancouver (http://www.meet-ics.com/wvac2 008/pdf/PS1-3June2008_003.pdf); Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors. There is the abstract about this article; Neurodegenerative diseases, including BSE, Alzheimer?s disease etc. are caused by different mechanisms but may share a final common pathway to neuronal injury due to the overstimulation of glutamate receptors, especially of the N-methyl-D -aspartate (NMDA) receptor subtype. It is generally accepted that the influx of Ca2+ as a result of excessive activation of the NMDA receptor underlies the toxic actions of glutamate in many systems. Also, ammonia intoxication leads to excessive activation of NMDA receptors in brain. On the other hand, Mg2+ competes with Ca2+ at voltage- gated calcium channels both intracellularly and on the cell surface membrane. So, Mg2+ can protect against NMDA- induced neurodegeneration and Ca2+ deficiency can be important about "NMDA hypofunction" in schizophrenia. There are no scientific references to date in which high intake of crude protein (and potassium) high enough to lead to a state of hyperammonemia (and hypomagnesemia) during the incubation period of the BSE. Therefore there is the first idea of this review; to show the hyperammonemia plus hypomagnesemia"simultaneo us" action on the ruminant tissues. Recently was found that elevated manganese in blood was associated with "prion infection" in ruminants. These findings about "manganese theory" act in concert with this "BSE ammonia- magnesium theory". Comments about this abstract; as a proof concerning Mg-deficiency (and hepatopathy; see www.bse-expert.cz ), according to the alternative BSE ammonia- magnesium theory; 1. In biological systems, only Mn2+ is readily capable of replacing Mg2+, and only in a limited set of circumstances. The body can replace Mn with Mg with similar efficiency in Mn-activated proteins (1990). Similarly, Mn can occupy Mg allosteric sites in Mg-activated proteins, such as the sarcoplasmic reticulum Ca- ATPase (1981). It was found (1999) that feeding rats a diet deficient in Mg; decreased urinary - fecal Mn excretion and greater Mn retention in skeletal muscle, heart and kidney (except the liver and trabecular bone) in Mg-deficient rats was observed. 2. Other cause about Mn deposits in tissues is liver disease. People with chronic liver disease have neurological pathology and behavioral signs of Mn neurotoxicity, probably because elimination of Mn in bile is impaired (1994- 1996). This impairment results in higher circulating concentrations of Mn, which then has access to the brain via transferrin. It was reported that whole blood Mn concentrations significantly increased in patients with chronic liver disease. Comments about recent ?Canada experiments? as another confirmation about the BSE ammonia- magnesium theory (hyperammonemia-proteinemia and hypomagnesemia) in the neurodegeneration; Normal prion protein (PrPc) might function to block some NMDA receptors and thereby prevent overexcitement and death of neurons. Recently researchers at the University of Calgary (April, 2008) found; when the nerve cells received the messenger glutamate, they went into hyperactive mode, however, when also Mg was removed from the cells, the brain cells went into seizure mode. Sincerely, Josef Hlasny, DVM, PhD, Czech Republic
Posted by hlasny, 19/11/2008 1:40:15 AM
Being a US rancher from ND, of all the cases of BSE that Canada had, they keep sending these old cows to the US that have turned into young cows with BSE. I feel the Canadian rancher has cost me my reputation as a cattle producer because they have not lived up to the feed band. I don't think that I should have to support the Canadian cattle industry by allowing their old and now young cows into the US and not being tested 100%, they are totally ruining my business because we are not able to export our beef which I consider free of BSE. This last case is where I draw the line. I will not support any more Canadian cattle coming to the US unless they are 30 months and under, I do not trust the canadian feed suppliers and rancher to quit using old feed that could be contaminated. It is just a matter of time before another BSE cow is shipped to the US and they will ruin our reputation again and we will pay the brunt of it.
Posted by don, 19/11/2008 11:04:39 AM

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